Electrical stimulation of the dorsal or median raphe nucleus in anesthetized rats produces a transient increase in arterial blood pressure. Heart rate and respiratory rate do not appear to change systematically after stimulation. Transections rostral or caudal to the raphe nucleus or electrolytic lesions of the nucleus linearis abolishes the pressor response to stimulation. Depletion of brain serotonin with PCPA significantly attenuates the pressor effect of both dorsal and median raphe stimulation. Fluoxetine, a specific serotonin uptake inhibitor, prolongs the duration of the raphe pressor effect and slightly increases its magnitude. Injections of the serotonin antagonist BOL into the anterior hypothalamus area significantly attenuates the dorsal raphe pressor effect whereas treatment of rats with the sympathetic postganglionic blocking agent bretylium prevents the stimulation induced pressor effect. Taken together these data suggest that stimulation of the ascending serotonergic neuronal system produces a phasic pressor effect which is mediated, at least in part, by synaptic serotonin.